Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotinamide (NAM, 1000 mg/kg), inosine (INS, 1000 mg/kg), hypoxanthine (HXT, 500 mg/kg), putative endogenous ligands of the benzodiazepine receptor, and nicotinic acid (NA, 500 mg/kg) diminished DL-kynurenine-(DL-K, 50 micrograms ICV) induced seizures in C57BL/6 adult male mice and only prolonged the latency of pentylenetetrazol (PTZ, 500 micrograms iCV) seizures. The same effect was previously observed when PTZ was administered IP. In albino male BALB/c and SHR (bred from Swiss) mice only NA was effective against DL-K. Diazepam in a dose of 0.5 mg/kg prevented PTZ-induced seizures in half of the animals but even in dose of 10 and 20 mg/kg it was ineffective against DL-K. When injected ICV NAM (1 and 10 micrograms), INS (10 micrograms) and HXT (10 micrograms) prevented seizures induced by DL-K and were ineffective against seizures induced by PTZ. It is suggested that if NAM, INS and HXT are of functional importance in the central nervous system, they can act as antagonists of endogenous brain kynurenine. NA and NAM are suggested to be functional feedback inhibitory regulators of the kynurenine pathway of metabolism of tryptophan.
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PMID:Nicotinamide, inosine and hypoxanthine, putative endogenous ligands of the benzodiazepine receptor, opposite to diazepam are much more effective against kynurenine-induced seizures than against pentylenetetrazol-induced seizures. 626 99

Phenibut, sodium hydroxybutyrate and baclofen are selectively effective against seizures induced in mice by the endogenous metabolites of tryptophan, L-kynurenine and quinolinic acid. The seizures were not affected by the drugs in doses under study. Depakine and aminooxyacetic acid as well as diazepam and phenobarbital appeared the most effective against pentylenetetrazole seizures. GABA and muscimol administered intracerebroventricularly merely prolonged the latency of seizures. Dissimilarities in the GABA-ergic mechanisms of the anticonvulsant effects of the drugs under consideration are discussed.
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PMID:[Convulsions induced by kynurenine and quinolinic acid as a sensitive test for assessing the anticonvulsant activity of GABA-ergic preparations]. 629 32

The effect of l-tryptophan in childhood hyperkinesia was compared with placebo tablets in 11 epileptic boys, aged 7-14 years, in a residential school for epileptics. The mean age of epilepsy was 2.5 years, and the duration of hyperactivity varied between 1.3 and 5.5 years. They were receiving either carbamazepine or sodium valproate alone, or combinations of both drugs for epilepsy. The investigation was designed as a double-blind cross-over study in which the patients were selected randomly to receive either l-tryptophan (40 mg/kg body weight) or matched placebo tablets first. Each treatment phase lasted for 5 weeks and the alternative medication was given after a 3-week washout period. Concomitant antiepileptic drugs were kept unaltered and no other drug was prescribed during the study. The patients were assessed at the pre-entry period (basal) and at the end of each treatment phase by their teachers and child care staff. The rating scale used included Connor's teacher and parent rating scales, the Meanwood Park Hospital behaviour scale, and visual analogue scales. A record of the patients' seizure frequency was kept throughout the investigation. Plasma antiepileptic drug levels were monitored at the end of each phase and they were virtually identical during these two treatment periods. In the dosage used, l-tryptophan was tolerated well by these children, and seizure frequency, as a whole, remained unaltered. However, no significant beneficial effect on their behaviour was observed during 5 weeks of l-tryptophan therapy.
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PMID:l-Tryptophan in hyperactive child syndrome associated with epilepsy: a controlled study. 642 13

Disulfiram prolonged the latency to clonic seizure caused by pentylenetetrazol (PTZ, 100 mg/kg SC). The effect of disulfiram was augmented by combination with tryptophan plus lithium, although neither tryptophan or lithium prolonged the latency to clonic seizure. The latency to tonic seizure was also prolonged in disulfiram-treated animals in parallel with the prolongation of the latency to clonic seizure. Lithium treatment completely prevented the incidence of tonic seizure, while this effect was cancelled in disulfiram-treated animals. Disulfiram acts on the clonic and tonic seizures in different ways.
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PMID:Effect of disulfiram in combination with L-tryptophan and lithium on pentylenetetrazol-induced seizure. 681 52

Pharmacological induction of changes in the serotonergic system was used to study the involvement of telencephalic serotonin (5-HT) in pinealectomy (PX) induced convulsions in the gerbil (Meriones unguiculatus). The reactions of the catecholamines norepinephrine (NE) and dopamine (DA) to both PX and drug treatment were also studied. Serotonin is apparently of little importance in the PX-induced convulsion since the artificial elevation by administration of tryptophan and 5-hydroxytryptophan, or depression by treatment with p-chloramphetamine, of telencephalic 5-HT had little effect on the convulsions. In other models for the study of epilepsy, lowered 5-HT results in an increase in seizure intensity. In this study, as in previous ones, telencephalic NE was repeatedly and significantly lowered after PX. None of the serotonergic drugs resulted in changes in NE. Data such as presented here are supportive of previous reports which indicate that a depression of NE facilitates convulsions.
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PMID:The involvement of brain amines in pinealectomy-induced convulsions in the gerbil: I. Serotonin. 697 73

A convulsant dose (100 mg/kg) of l-methionine-RS-sulphoximine (MSO) produced temporally correlated decreases in central 5-hydroxytryptamine (5-HT) and plasma and brain tryptophan (TRY) concentrations in C57BL/6J mice. In contrast, a subconvulsant dose of MSO (50 mg/kg) had no effect on central 5-HT levels and only decreased brain tryptophan at one time-point after its administration. The pattern of findings suggests that the decrease in central 5-HT levels resulting from a convulsant dose of MSO is related to an impairment in 5-HT synthesis resulting from a restriction of tryptophan availability. Administration of 25 mg/kg and 100 mg/kg doses of l-tryptophan with convulsant doses of MSO significantly increased seizure latency. It is suggested that the central 5-HT system modulates the expression of MSO-induced seizures.
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PMID:Tryptophan availability, central serotonergic function and methionine sulphoximine-induced convulsions. 706 6

L-glycine (1-12.5 micrograms, intracerebroventricularly, i.c.v.) completely prevented seizures induced by i.c.v. administration of L-kynurenine, and practically did not modify those induced by another convulsant quinolinic acid, a metabolite of tryptophan, and by strychnine. L-Glycine administered intraperitoneally (i.p.) (1000 mg/kg) decreased lethality after K-kynurenine and quinolinic acid; at doses of 3000 and 4000 mg/kg which are sedative and hypothermic it prolonged the latency of strychnine and L-kynurenine seizures. The convulsant action of pentylenetetrazol was not modified. Kynurenine seizures are suggested to be related to the action of kynurenine on glycine receptors in the central nervous system.
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PMID:Antagonism of L-glycine to seizures induced by L-kynurenine, quinolinic acid and strychnine in mice. 725 Feb 1

Intraventricular injection of DL-kynurenine and L-kynurenine sulfate (40 microgram) into conscious mice potentiated convulsions and lethality produced by strychnine (1 mg/kg) and not by thiosemicarbazide nor pentylenetetrazol. Another metabolite of tryptophan with convulsive effect, quinolinic acid, was ineffective. Intraperitoneal injection of DL-kynurenine sulfate and quinolinic acid (25-100 mg/kg) was associated with prolongation of the latency of strychnine and thiosemicarbazide (only the former drug) seizures. Nicotinic, picolinic, and anthranilic acids (100 and 250 mg/kg) did not modify the action of convulsants. Data and suggestions about probable involvement of brain glycine and gamma-aminobutyric acid receptors in the convulsive action of kynurenines is discussed.
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PMID:Effect of kynurenine and quinolinic acid on the action of convulsants in mice. 740 16

Taurine in doses of 100 and 200 mg/kg (intraperitoneally) and 2.5 micrograms (into brain ventricles) antagonized clonic seizures produced by L-kynurenine sulfate injected into brain ventricles of SHR adult male albino mice. Seizures produced by another metabolite of tryptophan in the kynurenine pathway, quinolinic acid, were intensified. The convulsant effects of strychnine, pentylenetetrazol and thiosemicarbazide was not modified.
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PMID:Taurine selectivity antagonizes L-kynurenine-produced seizures in mice. 742 78

Serotonin(5-HT) plays an important role in the seizures of El mice since the seizure threshold of El mice correlates with the 5-HT concentration in the central nervous system. In this study, the anticonvulsant effect of a 5-HT reuptake blocker, citalopram, was evaluated behaviorally and biochemically. El mouse convulsions were inhibited by oral administration of citalopram for 2 weeks. Citalopram increased tryptophan and tyrosine amounts, and decreased the 5-HT, 5-hydroxyindoleacetic acid, kynurenine, and dopamine amounts in the brain. These findings show that citalopram depresses monoaminergic metabolism. Given the known convulsant effect of kynurenine, it is suggested that its decrease by citalopram may involve attenuation of El mice seizures.
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PMID:The anticonvulsant effect of citalopram on El mice, and the levels of tryptophan and tyrosine and their metabolites in the brain. 752 May 38


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